Complications of Myocardial Infarction

Left Ventricular (LV) Thrombus

  • LV thrombus is usually seen in patients presenting with large anterior STEMI’s.
    • Late presentation is an important risk factor
  • LV thrombus results from the perfect storm of factors contributing to “Virchows Triad”:
    • LV wall akinesis/dyskenia resulting in stagnant blood flow
    • Pro-coagulative state
    • Inflammation (due to ischemia)
  • The incidence of LV thrombus is about 5-7% in anterior MI. 
    • (number may be smaller with modern reperfusion times)
  • Imaging options:
    • Echo (most commonly used)
    • CT, or MRI.
  • LV thrombus forms 12-72hrs after MI.
    • Imaging too early in their MI course may not identify an LV thrombus

Treatment of LV Thrombus

  • The most dreaded complication of LV thrombus is stroke.
  • Anticoagulation
    • Vitamin K antagonists
    • DOACs are available, but only used if VKA intolerant (no clinical trials available, case reports only)
  • Primary Prevention in Anterior MI
    •  CCS 2018 – No routine anticoagulation (citing poor evidence and high risk of bleeding)
    • AHA 2013 – Class IIB indication for anticoagulation
  • Generally treat with anticoagulation for 3-6 months with a repeat echo to reassess that the LV thrombus has resolved.
CCS 2018 Heart Failure Guidelines
  • We recommend against routine anticoagulation after large anterior MI and low EF, in the absence of intracardiac thrombus or other indications for anticoagulation (Weak Recommendation; Low-Quality Evidence).
AHA 2013 STEMI Guidelines
  • Anticoagulant therapy may be considered for patients with STEMI and anterior apical akinesis or dyskinesis. (Class IIB) (Level of Evidence: C)
    (Duration: 3 months.  INR 2.0-2.5 if used with DAPT)

Left Ventricular Aneurysm and Pseudoaneurysm

  • Left ventricular aneurysm
    • Result of thinning of the myocardium.
    • Identified by a large neck.
    • Low risk of rupture
    • Persistent ST elevation on their EKG.
  • Left ventricular pseudoaneurysm
    • Cardiac myocardial rupture that is contained by the pericardium
    • Very narrow neck
    • High risk for rupture -> increased mortality

Right Ventricular (RV) Infarct

  • Complication of inferior STEMI’s.
  • No RV contractility to maintain forward flow, which leads to LV underfilling (reduced preload), reduced cardiac output, and hypotension.
    • Drugs that further reduce preload such as nitrates and diuretics can worsen cardiac output leading to more hypotension and shock.
  • RV is supplied mostly by the RV branch of the RCA.  Proximal RCA lesion can compromise the RV branch. 
  • Important for early recognition and diagnosis of RV infarct.

EKG Findings in RV Infarct

  • Indirect Evidence of RV Infarction:
    • ST elevation in lead III > Lead II   (Suggests RCA occlusion)
    • ST elevation in V1 (Remember V1 is closest to the RV on a typical 12 lead EKG).
    • ST elevation in V1 but ST depression in V2 -> suggestive of RV infarct.
  • Direct Evidence of RV Infarction
    • ST elevation in V4R (15 lead EKG is required). V4Reverse puts a lead directly over the RV.
    • Remember only 0.5mm of ST elevation is required to be considered positive in V4R.

Cath

  • RCA lesions are most common reason for RV infarct as the RV branch is supplied by the RCA.
  • Usually very proximal lesions.
Inferior STEMI with RV infarct

ECHO

  • Can be useful in assessing the severity of an RV infarct.
    1. Visual qualitative assessment. 
    2. TAPSE (Tricuspid Annular Plane Systolic Excursion) has been a validated tool to assess RV function.
      • Involves am M-mode at the base of the RV to assess tricuspid annular motion.
      • Normal ≥ 1.7 cm.
      • TAPSE has been validated as a predictor of heart failure and survival.
    3. Tissue Doppler
      • Systolic excursion (S’) of < 9.5 cm/sec is suggestive of RV dysfunction.

RV Infarct on ECHO

Management

  • Revascularization
    • Even after revascularization, the right ventricle may take some time to recover.
  • Hypotension Management
    • The main hemodynamic problem resulting from an RV infarction is reduced LV preload, which causes reduced cardiac output/shock and hypotension.
    • Avoid therapies that further reduce preload (nitrates, narcotics, propofol, etc.)
    • Use therapies to improve preload (IV fluids, vasopressors)
  • Dobutamine
    • Improves RV stroke volume, and improves RV afterload by reducing pulmonary vascular resistance
    • Ideally used after revascularization because inotropes can cause complications during acute MI (arrhythmias, increase in infarct size, etc.)
 

Heart Block

Inferior Infarct related heart block:

  • Usually RCA, rarely can be circumflex.
  • Heart block associated with high-vagal tone Bezold-Jarisch reflex or rarely from AV node ischemia
  • Often transient and can be treated with atropine.
  • Pacemaker should generally be avoided due to risk of RV perforation (can be placed in extreme circumstances)

Anterior Infarct related heart block:

  • Usually related to extensive infarct and damage to the conduction system in the septum.
  • Complete heart block often preceded by RBBB + LAFB.
  • Temporary/permanent pacemaker more likely to be required usually see more distal conduction disease like Mobitz 2, third degree heart block, or alternating bundle branch blocks.
Inferior STEMI with Wenkebach

Ventricular Septal Defect

  • A very uncommon complication of acute MI.
  • Typically seen in late presenting patients who have not been revascularized. They are often female, older patients, and have no history of MI/Angina prior to presentation (less collaterals).
  • Often have poor prognosis.

Types

  1. Anterior Infarct often located at the apical ventricular septal.
  2. Inferior Infarct often located at the inferobasal ventricular septum. Usually a worse prognosis.

Clinical Features

  • Prominent pan-systolic murmur at left lower sternal border often associated with a thrill.
  • Signs of right sided heart failure, pulmonary edema or shock.
  • Echo helps confirm evidence of a VSD with left to right shunt as well as complications such as RV failure.

Management

  • Hemodynamic support with ionotropes, afterload reduction with nitroprusside and can consider IABP for mechanical support as bridge to surgery.
  • Surgical closure or percutaneous options.

Myocardial Rupture

  • Uncommon complication but very high mortality.
  • The risk factors are similar to VSD’s. Patients are often older, late presenting, female, first presentation MI (lack of collaterals).
  • Patients can have sudden PEA arrest from cardiac tamponade.
  • Myocardial rupture is typically preceded by pain similar to the patients initial presentation.
  • Hypertension, excessive straining, coughing, or vomiting may be triggers.

Management

  • Cardiac Arrest -> Standard ACLS plus pericardiocentesis.
  • Hemodynamic compromise -> Fluids, dobutamine/pressors, pericardiocentesis.
  • Traditionally there was concern regarding pericardiocentesis in that performing it would leave to clot dislogement and worsen leak. However, if there is hemodynamic compromise a pericardiocentesis should be performed, minimal fluid should be removed in order to restore hemodynamics (10-50ml).
  • Surgical consultation is a must. Teflon or pericardial patch can be performed on the epicardium to stabilize the rupture.

Papillary Muscle Rupture

  • Presentation:
    • Pulmonary edema
    • Hypotension
    • Shock
    • Murmur may not be very loud (because of rapid equalization of pressures across the mitral valve) but patients will have severe MR.
  • Posteromedial papillary muscle
    • Most common
    • Single blood supply PDA.
  • Anterolateral papillary muscle
    • Dual blood supply from the LAD and Circumflex.
  • Treatment
    • Inotropes
    • IABP
    • URGENT Surgical Consult

Transthoractic Echo

Transesophageal Echo

References

  • Figueras J, Cortadellas J, Soler-Soler J Left ventricular free wall rupture: clinical presentation and management

Contributors

  • Primary Author: Dr. Daniel Durocher (MD FRCPC)
  • Reviewers:
    • Dr. Pavel Antiperovitch (MD, FRCPC)
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